Department of Pathophysiology, Jagiellonian University, Medical College, Cracow, Poland.
J Physiol Pharmacol. 2011 Jun;62(3):321-6.
The study investigated the mechanisms through which the hyperosmolarity might induce detrusor overactivity (DO). We compared the bladder activity in response to partial and complete blockade of TRPV1-6 and TRPA1 receptors. Experiments were performed on 42 rats. DO was induced by using hyperosmolar saline. All animals were randomly divided into six groups. The measurements represent the average of five bladder micturition cycles. Hyperosmolar saline induced DO. The complete blockade of TRPV1-6 and TRPA1 prevented DO. The partial blockade of TRPV1 didn't prevented DO. In the voiding phase periodical bladder contractions complexes occurred leading to slow urine flow due to bladder distension. Ruthenium red and capsaicin resulted in complete disorganisation of detrusor muscle contractility impairing urine voiding and leading to constantly lasting urine retention in healthy rats.
hyperosmolar-induced DO is mediated by TRPV and TRPA1 channels; the hyperosmolar stimuli of urinary bladder might be transmitted mostly via ruthenium red sensitivity pathway.
本研究旨在探讨高渗状态诱导逼尿肌过度活动（DO）的机制。我们比较了部分和完全阻断 TRPV1-6 和 TRPA1 受体后膀胱活动的变化。实验在 42 只大鼠上进行。使用高渗盐水诱导 DO。所有动物随机分为六组。测量结果代表五次膀胱排尿周期的平均值。高渗盐水诱导 DO。完全阻断 TRPV1-6 和 TRPA1 可预防 DO。部分阻断 TRPV1 并不能预防 DO。在排尿期，周期性的膀胱收缩复合物导致膀胱扩张导致尿流缓慢。钌红和辣椒素导致逼尿肌收缩力完全紊乱，损害排尿功能，并导致健康大鼠持续的尿潴留。
高渗诱导的 DO 是由 TRPV 和 TRPA1 通道介导的；膀胱的高渗刺激可能主要通过钌红敏感性途径传递。
